This study seeks to validate an approach to cancer chemotherapy based on the interruption of gluconeogenesis at the phosphoenolpyruvate carboxykinase (PEP CK) and pyruvate carboxylase (PC) levels, and thus represents an attack on the host's thermodynamic participation in the malignant process. Specifically, inhibition of gluconeogenesis (in normal tissues: liver, kidney cortex) is aimed at retarding host energy loss (and therefore cancer cachexia) attendandt upon the disease. It is proposed that since host energy loss (cachexia) and tumor energy gain (tumor growth) appear to be functionally (i,e., systemically) interrelated, a block to one may result in a block to the other; thus agents which interfere with gluconeogenesis in the host may also interfere with tumor growth itself. Initial experimental results confirm that inhibitors of PEP CK and PC produce tumor inhibition in the growth of various in-vivo transplantable animal tumors. Such experiments will be expanded as this study progresses. Emphasis will be placed on the concurrent exploration of exact biochemical mechanisms operative during the course of administration of gluconeogenic blocking agents.